The physiological role of methyl group oxidation by sarcosine dehydrogenase has been evaluated through studies of a patient with proven sarcosine dehydrogenase deficiency. The patient was allowed to attain a physiological steady state upon a series of fixed diets containing varying amounts of methionine, choline (or its structural analogues), and glycine. Sarcosine, creatinine, creatine, and total nitrogen and sulfur excretions were measured. The results obtained permit formulation of a quantitative model of methyl group metabolism in the human under a variety of nutrional conditions. This model suggests that transmethylation reactions forming creatine and a variety of other metabolites impose demands for labile methyls which are somewhat in excess of the supply of labile methyls ingested as methionine and choline. Under such conditions methylation glycine to form sarcosine is minimal. When labile methyls are ingested in excess of these fixed requirements, methylation of glycine with subsequent oxidation of sarcosine serves as the chief pathway of disposal of these excess methyl moieties.